ライフサイエンスコーパス: B. pertussis

1 B. pertussis also requires a relatively expensive growth

2 B. pertussis and B. bronchiseptica core OS were bound to

3 B. pertussis does not express the O antigen, while B. pa

4 B. pertussis encodes many uncharacterized transcription

5 B. pertussis grew efficiently and caused moderate pathol

6 B. pertussis uses pertussis toxin (PT) and adenylate cyc

7 B. pertussis virulence factor tracheal cytotoxin (TCT),

8 B. pertussis was confirmed in all cases.

9 B. pertussis-induced histamine sensitization (Bphs) is a

10 B. pertussis-infected pendrin knockout (KO) mice had hig

11 B. pertussis-stimulated dendritic cells from IL-1R(-/-)

12 el of conservation of gene content among 137 B. pertussis strains with different geographical, tempor

13 Only 16 (38%) B. pertussis-associated hospitalizations fulfilled the C

14 b specimens containing as few as 1.8 x 10(6) B. pertussis genomes/mL and showed no false-positives.

15 Sixty of 72 B. pertussis isolates were viable for analysis.

16 ted by the LFIA were conserved in 98% of 954 B. pertussis isolates collected across 12 countries from

17 measure of in vivo fitness, the ability of a B. pertussis heme utilization mutant to colonize and per

18 P phosphatase activity by NSC87877 abrogated B. pertussis survival inside murine macrophages.

19 Acellular B. pertussis vaccines were not efficiently protective ag

20 these are novel for responses to penta-acyl B. pertussis LPS, and their mutation does not affect the

21 suggests that recognition of penta-acylated B. pertussis lipid A is dependent on uncharged amino aci

22 Functionality of antibodies against B. pertussis was measured using B. pertussis growth inhi

23 e-induced antisera were bactericidal against B. pertussis, and the titers correlated with ELISA-measu

24 a saline solution, were bactericidal against B. pertussis, and their titers correlated with their ELI

25 ter vaccinations were more effective against B. pertussis than B. holmesii (effectiveness: 67% and 36

26 ion in adaptive immunological memory against B. pertussis.

27 hat BPZE1 induces protection in mice against B. pertussis within days after vaccination, at a time wh

28 vaccine candidate induces protection against B. pertussis and prevents nasal colonization in animal m

29 ntigens, confer efficient protection against B. pertussis but not against B. parapertussis.

30 s strong and long-lasting protection against B. pertussis challenge by inducing potent Ab and T cell

31 ving vaccine efficacy and protection against B. pertussis transmission.TRIAL REGISTRATIONClinicalTria

32 ines were not efficiently protective against B. pertussis in IL-1R(-/-) mice.

33 and suppress innate immune responses against B. pertussis infection.

34 ophil recruitment, which consequently allows B. pertussis to avoid rapid antibody-mediated clearance

35 ussis and Bordetella bronchiseptica Although B. pertussis represents a pathogen strictly adapted to t

36 the in vivo fitness of B. bronchiseptica and B. pertussis.

37 protects against both pertussis disease and B. pertussis infection.

38 Symptoms were similar among B. holmesii- and B. pertussis-infected patients.

39 on systems in mice, sera from uninfected and B. pertussis-infected human donors were screened for ant

40 The two conjugates induced similar anti-B. pertussis LPS IgG levels in mice.

41 Molecular characterization of archived B. pertussis isolates (collected January 2007 to March 2

42 results that were incorrectly identified as B. pertussis by the FilmArray RP and one false-negative

43 of other Bordetella species misidentified as B. pertussis during a period of increased pertussis inci

44 ti-inflammatory properties of the attenuated B. pertussis BPZE1 vaccine candidate and supports its de

45 ectrum antibiotic treatment delivered before B. pertussis inoculation reduced the infectious dose to

46 rences in low-temperature adaptation between B. pertussis and B. bronchiseptica may result from selec

47 d Aries Bordetella Assay, which detects both B. pertussis and B. parapertussis directly from nasophar

48 e upregulated during iron starvation in both B. pertussis strain Tohama I and Bordetella bronchisepti

49 rdetella species (Bordetella bronchiseptica, B. pertussis, and B. parapertussis) and its role in thei

50 Alcaligin-mediated iron acquisition by B. pertussis may be critical for successful host coloniz

51 d by PRN(-) B. pertussis and cases caused by B. pertussis producing pertactin (PRN(+)) (P = .01).

52 Biofilm formation by B. pertussis plays an important role in pathogenesis.

53 ntly to the inflammatory response induced by B. pertussis infection by augmenting COX-2 expression an

54 However, immunity induced by B. pertussis infection prevented subsequent B. pertussis

55 Ptx contributes to IL-1beta induction by B. pertussis, which is involved in IL-10 induction throu

56 ment enhanced respiratory tract infection by B. pertussis, even though it also induced a rapid influx

57 was induced in the lungs of C57BL/6 mice by B. pertussis.

58 ssis toxin (Ptx), which is expressed only by B. pertussis.

59 ourse and were less efficiently protected by B. pertussis vaccination than wild-type mice.

60 early infection of the respiratory tract by B. pertussis.

61 control infection but did not rapidly clear B. pertussis from the lungs.

62 We characterized 703 clinical B. pertussis isolates collected in the United Kingdom be

63 Under iron starvation stress conditions, B. pertussis produces the siderophore alcaligin.

64 ay is useful as a diagnostic tool to confirm B. pertussis infections and to rapidly identify other Bo

65 pharyngeal samples with previously confirmed B. pertussis or B. parapertussis data and with data from

66 Curiously, B. pertussis-infected IFNAR1 knockout mice had wild-type

67 pertactin-producing and pertactin-deficient B. pertussis infections.

68 An isogenic Ptx-deficient B. pertussis strain had only a modest phenotype in wild-

69 ith wild-type (WT) or PT-deficient (DeltaPT) B. pertussis.

70 ped a multitarget PCR assay to differentiate B. pertussis, B. holmesii, and B. parapertussis and prov

71 Of the USPHLs that differentiated B. pertussis and B. holmesii, sensitivity was 96% and sp

72 tively, 72% and 79% of USPHLs differentiated B. pertussis and B. holmesii and 68% and 72% identified

73 ular assays in detecting and differentiating B. pertussis and B. parapertussis in nasopharyngeal swab

74 organisms, but did react with nine distinct B. pertussis strains.

75 t lower levels of IL-10 were detected during B. pertussis infection in IL-1R(-/-) mice.

76 ls deregulate immune system functions during B. pertussis infection.

77 gly, we found no role for neutrophils during B. pertussis infection in naive mice.

78 er neutrophils play a protective role during B. pertussis infection in mice.

79 t effects of type I/III IFN signaling during B. pertussis infection and suggest that these pathways r

80 jacking of SHP-1 by CyaA action then enables B. pertussis to evade NO-mediated killing in sentinel ce

81 CyaA-produced signaling of cAMP thus enables B. pertussis to evade the key innate host defense mechan

82 o the circulation, significantly exacerbated B. pertussis infection.

83 In support of this finding, B. pertussis-infected mice with a knockout mutation in t

84 he reference assays were 97.1% and 99.0% for B. pertussis and 100% and 99.7% for B. parapertussis The

85 f detection (LoDs) were 1,800 CFU.ml(-1) for B. pertussis and 213 CFU.ml(-1) for B. parapertussis The

86 n) LFIA detection of TcfA as a biomarker for B. pertussis infection is feasible and may facilitate ea

87 LODs) were 150 CFU/ml or 3 fg/mul of DNA for B. pertussis and 1,500 CFU/ml or 10 fg/mul of DNA for B.

88 sted at two U.S. commercial laboratories for B. pertussis and B. parapertussis detection.

89 Our data reveal a biofilm lifestyle for B. pertussis in the nose and the requirement of Bps in t

90 PA) and negative percent agreement (NPA) for B. pertussis were 98.7% and 97.3%, respectively.

91 A total of 171 patients tested positive for B. pertussis from 1 March to 31 October 2010 by polymera

92 As shown previously for B. pertussis, bfrD expression in B. bronchiseptica was a

93 uence 481 (IS481), which is not specific for B. pertussis; therefore, the relative contribution of ot

94 t the time of illness visits were tested for B. pertussis by polymerase chain reaction (PCR).

95 teria of respiratory illness were tested for B. pertussis infection by PCR on paired NPSs and NPAs; o

96 tics of nucleic acid amplification tests for B. pertussis.

97 PAs), and induced sputum, have been used for B. pertussis detection, although there is limited head-t

98 rtance of alcaligin and haem utilization for B. pertussis in vivo growth and survival.

99 IS481 cycle threshold (CT) values for B. pertussis samples had coefficients of variation (CV)

100 pertussis to colonize mice convalescent from B. pertussis infection.

101 with illness, 0.7 percent to 5.7 percent had B. pertussis infection, and the percentage increased wit

102 ronchiseptica) and whooping cough in humans (B. pertussis and B. parapertussis).

103 mics analysis, potentially novel immunogenic B. pertussis antigens were identified.RESULTSAll BPZE1 v

104 In B. pertussis, BtrA retains activity as a BtrS antagonist

105 In B. pertussis, deletion of the rseA gene results in high

106 In B. pertussis-infected mice, lung type I/III IFN response

107 Most importantly, deletion of btrA in B. pertussis revealed T3SS-mediated, BteA-dependent cyto

108 ted, inactivated, or unregulated by BvgAS in B. pertussis.

109 system; however, in contrast to the case in B. pertussis, the known modulators nicotinic acid and su

110 le cells that incorporated 3OH-C12 chains in B. pertussis lipid A.

111 ich specifically attaches 3OH-C12 chains, in B. pertussis This expression was lethal, suggesting that

112 resent study examined genome-wide changes in B. pertussis gene transcript abundance in response to ir

113 All three genes are highly conserved in B. pertussis, B. parapertussis, and B. avium.

114 ernative mechanisms to oxidize disulfides in B. pertussis are analyzed and discussed.

115 iplex assay include IS481, commonly found in B. pertussis and B. holmesii; IS1001 of B. parapertussis

116 Expression of meningococcal LpxH in B. pertussis indeed resulted in new symmetric lipid A sp

117 zymes in the lipid A biosynthesis pathway in B. pertussis cannot handle precursors with a 3OH-C12 cha

118 d that localization of PtlH was perturbed in B. pertussis strains that were treated with carbonyl cya

119 indicating that gene acquisition is rare in B. pertussis.

120 Comparative analysis of Bvg regulation in B. pertussis and B. bronchiseptica revealed a relatively

121 iple aspects of adaptive immune responses in B. pertussis-infected IL-6(-/-) mice and suggest that IL

122 ining pulmonary transcriptional responses in B. pertussis-infected mice treated with S1PR agonist AAL

123 r sphingosine-1-phosphate (S1P) signaling in B. pertussis-mediated pathology and highlight the possib

124 results indicate a role for S1P signaling in B. pertussis-mediated pathology and highlight the possib

125 in vivo technology (RIVET) system for use in B. pertussis.

126 the lipid A biosynthesis pathway, which, in B. pertussis, has limited chain length specificity.

127 These heat-inactivated B. pertussis Ag/LPS-stimulated mast cells fail to promot

128 tella bronchiseptica cluster, which includes B. pertussis, B. parapertussis, and B. bronchiseptica.

129 with other classical bordetellae, including B. pertussis and B. parapertussis, something the current

130 2% (n = 99) were identified as indeterminate B. pertussis at CDC.

131 During infection, B. pertussis releases several toxins, including pertussi

132 Klebsiella species was sufficient to inhibit B. pertussis colonization of antibiotic-treated mice.

133 Interestingly, an isogenic B. pertussis strain lacking pertussis toxin did not indu

134 ce produced IL-17 in response to heat-killed B. pertussis in the presence of APC.

135 ting that interspecies competition may limit B. pertussis colonization of mice.

136 om the human lower respiratory tract limited B. pertussis growth in vitro, indicating that interspeci

137 enting apoptosis induced by exposure to live B. pertussis.

138 W contained up to approximately 10(8) CFU/ml B. pertussis and 1 to 5 ng/ml ACT at the peak of infecti

139 Interestingly, B. parapertussis, but not B. pertussis, produces an O antigen, a factor shown in o

140 The incidence (per 1000) of B. pertussis-associated hospitalization was 2.9 (95% con

141 anges in genome-wide transcript abundance of B. pertussis as a function of growth phase and availabil

142 The adenylate cyclase toxin (ACT) of B. pertussis is a potent enzyme that converts cytosolic

143 tica may result from selective adaptation of B. pertussis to the human host.

144 ions as an adhesin by promoting adherence of B. pertussis and Escherichia coli to human nasal but not

145 An exploratory analysis of B. pertussis culture was performed on induced sputum spe

146 ystem protein production by an assortment of B. pertussis laboratory-adapted and low-passage clinical

147 We conclude that the asymmetry of B. pertussis lipid A is determined by the acyl chain len

148 this defect as well as for the asymmetry of B. pertussis lipid A.

149 rable host microbiota, whereas 10 000 CFU of B. pertussis were required to colonize murine nasal cavi

150 sis antibodies and reduce the circulation of B. pertussis.

151 -type mice in their control and clearance of B. pertussis or B. parapertussis, suggesting that IgA is

152 required for antibody-mediated clearance of B. pertussis.

153 surveillance with laboratory confirmation of B. pertussis infection, we cannot definitively conclude

154 of pertussis toxin, allowing both control of B. pertussis numbers and regulation of the inflammation

155 e defect of IL-6(-/-) mice in the control of B. pertussis numbers.

156 were admitted to hospital within 21 days of B. pertussis detection, whereas none of the 20 cases >/=

157 other molecular assays for the detection of B. pertussis and B. parapertussis.

158 tum performed similarly for the detection of B. pertussis infection in young infants by PCR.

159 ies BA and FilmArray RP for the detection of B. pertussis was considered good at 97.7% with a kappa v

160 assays to improve the molecular detection of B. pertussis.

161 283 and BP485, for the specific detection of B. pertussis.

162 ovides accurate detection and distinction of B. pertussis and B. parapertussis infections within 2 h.

163 heir coexistence and the limited efficacy of B. pertussis vaccines against B. parapertussis suggest a

164 In attempts to modulate the endotoxicity of B. pertussis lipid A, here we expressed the gene encodin

165 variety of approaches to examine features of B. pertussis genetic variation.

166 ligin transport to the ecological fitness of B. pertussis may be important for adaptation to iron-res

167 of the enterobactin system to the fitness of B. pertussis was confirmed using wild-type and enterobac

168 ation, while knockout of the BpeGReg gene of B. pertussis results in decreased biofilm formation.

169 st to our previous report, the fhaB genes of B. pertussis and B. bronchiseptica are functionally inte

170 We also show that the cyaA genes of B. pertussis and B. bronchiseptica, which encode adenyla

171 evious studies showed that the fhaB genes of B. pertussis and B. bronchiseptica, which encode filamen

172 In this study, the bfrD and bfrE genes of B. pertussis were shown to be functional in B. bronchise

173 ntly specific for reliable identification of B. pertussis.

174 Imaging of B. pertussis-exposed neutrophils revealed that B. pertus

175 uld contribute to the increased incidence of B. pertussis infection since the transition to the use o

176 Isolation of B. pertussis in adults is difficult, resulting in a dela

177 The lipopolysaccharide (LPS) of B. pertussis is an attractive antigen for vaccine develo

178 both gene and protein levels in the lungs of B. pertussis-infected mice.

179 curated flux balance analysis-based model of B. pertussis metabolism.

180 Adacel vaccines contain high copy numbers of B. pertussis DNA, which can be aerosolized, causing fals

181 eport the first documented mixed outbreak of B. pertussis and B. holmesii infections.

182 ilization contributes to the pathogenesis of B. pertussis in the mouse infection model and indicate t

183 central role of CyaA in the pathogenesis of B. pertussis.

184 enzymatic activity inhibits phagocytosis of B. pertussis in vitro.

185 We show that the Bps polysaccharide of B. pertussis is critical for initial colonization of the

186 duction requires growing large quantities of B. pertussis.

187 to investigate BvgAS-mediated regulation of B. pertussis virulence factors in vivo using the mouse a

188 n between neonatal mice, the first report of B. pertussis transmission in mice.

189 etics of BvgA phosphorylation after shift of B. pertussis cultures from non-permissive to permissive

190 In the virulent phase, the default state of B. pertussis, the cytoplasmic enzymatic moiety of BvgS a

191 ner membrane fractions of a mutant strain of B. pertussis that does not produce PT.

192 ately 10(8) CFU/ml of a laboratory strain of B. pertussis was cultured in vitro, ACT production was d

193 raction of the cell in a wild-type strain of B. pertussis.

194 bcellular localization of PtlH in strains of B. pertussis lacking PT, lacking other Ptl proteins, or

195 eting cellular ATP levels, and in strains of B. pertussis that produce an altered form of PtlH that l

196 We have previously shown that two strains of B. pertussis, BP338 (a Tohama I-derivative) and 18-323,

197 could recognize multiple clinical strains of B. pertussis, highlighting the potential of Qbeta-glycan

198 to how it localized in wild-type strains of B. pertussis, PtlH exhibited aberrant localization in st

199 rrelate to the in vivo expression studies of B. pertussis iron systems in mice, sera from uninfected

200 me utilization contributed to the success of B. pertussis as a pathogen.

201 tive results that can, given the tendency of B. pertussis to cause outbreaks, result in unnecessary a

202 is that is similar but distinct from that of B. pertussis.

203 h it is widely believed that transmission of B. pertussis occurs via aerosolized respiratory droplets

204 In addition, treatment of B. pertussis-infected mice with the carbonic anhydrase i

205 indicating that the particular virulence of B. pertussis in these mice requires Ptx.

206 tinct, and current vaccines, containing only B. pertussis-derived antigens, confer efficient protecti

207 heat-killed whole-cell B. bronchiseptica or B. pertussis inhibited shedding of B. bronchiseptica.

208 The overall B. pertussis PCR positivity was 2.3% (42/1839), of which

209 By comparing parental B. pertussis to an rseA gene deletion mutant (PM18), we

210 quired for persistence of the human pathogen B. pertussis in the murine LRT and we provide evidence t

211 xacerbated host airway responses during peak B. pertussis infection but also may inhibit host mechani

212 h can be aerosolized, causing false-positive B. pertussis PCR results.

213 eal that resident microorganisms can prevent B. pertussis colonization and influence host specificity

214 trategy in a setting such us ours to prevent B. pertussis-associated illness in women and their young

215 tion differed between cases caused by PRN(-) B. pertussis and cases caused by B. pertussis producing

216 cine dose had a higher odds of having PRN(-) B. pertussis compared with unvaccinated case-patients (a

217 rmining whether pertactin-deficient (PRN(-)) B. pertussis is evading vaccine-induced immunity or alte

218 pertactin-deficient and pertactin-producing B. pertussis infection in infants and describe correspon

219 deficient and those with pertactin-producing B. pertussis.

220 ile B. bronchiseptica has a wide host range, B. pertussis and B. parapertussis evolved separately fro

221 , though lower in titer, efficiently reduced B. pertussis numbers in IL-6-sufficient mice.

222 IL-10 treatment reduced B. pertussis numbers in IL-1R(-/-) mice, suggesting that

223 compared with B. bronchiseptica Remarkably, B. pertussis maintained the production of virulence fact

224 ied.RESULTSAll BPZE1 vaccinees showed robust B. pertussis-specific antibody responses with regard to

225 eased type I IFN receptor (IFNAR) signaling, B. pertussis infection exacerbated lung inflammatory pat

226 als and wP-vaccinated animals possess strong B. pertussis-specific T helper 17 (Th17) memory and Th1

227 B. pertussis infection prevented subsequent B. pertussis infections but did not protect against B. p

228 In response to low temperatures, B. pertussis adapted its fatty acid composition and memb

229 tibody levels (p < 0.001) against all tested B. pertussis antigens post-priming compared to 157 infan

230 ntibody levels (P < .001) against all tested B. pertussis antigens postpriming compared to 157 infant

231 stantially earlier in B. bronchiseptica than B. pertussis following a switch from Bvg(-) to Bvg(+) ph

232 vestigated because it is easier to grow than B. pertussis.

233 expression among Bordetella species and that B. pertussis is capable of expressing a full range of T3

234 Given that B. pertussis is thought to have derived from a Bordetell

235 tin and haem, supporting the hypothesis that B. pertussis is iron-starved and responds to the presenc

236 rtussis proteins support the hypothesis that B. pertussis perceives an iron starvation cue and expres

237 pertussis-exposed neutrophils revealed that B. pertussis lacking ACT induces formation of neutrophil

238 data suggest increasing selection among the B. pertussis population in Australia in favor of strains

239 . bronchiseptica bvgAS mutant expressing the B. pertussis bvgAS genes revealed that the interspecies

240 481, which is present in high numbers in the B. pertussis chromosome.

241 t IS481, present in 218 to 238 copies in the B. pertussis genome and 32 to 65 copies in B. holmesii.

242 re sugars and unusual glycosyl linkages, the B. pertussis LPS is a highly challenging synthetic targe

243 mouse respiratory model, inactivation of the B. pertussis ferric alcaligin receptor protein was found

244 tenuation resulting from inactivation of the B. pertussis heme system was assessed using mixed infect

245 e propose that the reduced plasticity of the B. pertussis membranes ensures sustained production of v

246 al evidence of the in vivo importance of the B. pertussis receptors was obtained from serologic studi

247 pertussis patient serum reactivity with the B. pertussis BfrD and BfrE proteins.

248 infection model showed that several of these B. pertussis iron systems are required for colonization

249 d natural-host animal models should apply to B. pertussis FHA as well.

250 parameters: IgG, IgA, and memory B cells to B. pertussis antigens.

251 gAS alleles of B. bronchiseptica compared to B. pertussis, but appears to be species specific.

252 d capacity in B. bronchiseptica, compared to B. pertussis, for ex vivo adaptation.

253 sA regulon adds a new layer of complexity to B. pertussis virulence gene regulation.

254 r Toll-like receptor 4 (TLR4) in immunity to B. pertussis and B. bronchiseptica, while no role for TL

255 immunity to B. pertussis Natural immunity to B. pertussis induced by infection is considered long las

256 of respiratory CD4 TRM cells in immunity to B. pertussis Natural immunity to B. pertussis induced by

257 e immune response and restored resistance to B. pertussis infection.

258 nd T cell cytokine production in response to B. pertussis as well as the generation of effective vacc

259 upregulate type I or III IFNs in response to B. pertussis infection and were protected from lethal in

260 needed to understand the immune response to B. pertussis infection in children vaccinated with aP va

261 ich reduces neutrophil influx in response to B. pertussis infection, potentially providing an advanta

262 rophages and other lung cells in response to B. pertussis infection.

263 nts impaired their innate immune response to B. pertussis infection.

264 flux to the lungs and airways in response to B. pertussis respiratory tract infection in mice.

265 Enhanced innate immune response to B. pertussis was characterized by increased production o

266 factor, in lung transcriptional responses to B. pertussis infection in mouse models.

267 ic or pulmonary T cell cytokine responses to B. pertussis, including Th1 and Th17 cytokine production

268 ader and different antibody specificities to B. pertussis antigens as compared with the aPV that prim

269 that controls differential susceptibility to B. pertussis PTX-induced HA sensitization (Bphs).

270 r bfrE imparted catecholamine utilization to B. pertussis.

271 than naive animals, and readily transmitted B. pertussis to unvaccinated contacts.

272 the attachment and phagocytosis of wild-type B. pertussis and FHA mutants.

273 xtracellular traps (NETs), whereas wild-type B. pertussis does not, suggesting that ACT suppresses NE

274 us macaques and olive baboons with wild-type B. pertussis strains and evaluated animals for clinical

275 Unfortunately, B. pertussis has relatively slow growth in culture, with

276 arapertussis The assay detected 16/18 unique B. pertussis/B. parapertussis strains.

277 Using B. pertussis cytochrome c4 as a reporter for cytochromes

278 dies against B. pertussis was measured using B. pertussis growth inhibition assay (BGIA).

279 Previous studies using B. pertussis and cultured mammalian cells identified sev

280 lenged with a high dose of a highly virulent B. pertussis isolate, they were fully protected against

281 Finally, coadministration of virulent B. pertussis with BPZE1 did not cause exacerbated outgro

282 mised MyD88-deficient mice, whereas virulent B. pertussis caused a severe pathological condition and

283 with suspected pertussis, 3.0% (n = 32) were B. pertussis positive and 0.2% (n = 2) were B. parapertu

284 ate or negative results, 46.1% (n = 53) were B. pertussis positive when tested by an alternate master

285 These CD4 TRM cells were B. pertussis specific and secreted IL-17 or IL-17 and IF

286 ient availability may serve as cues by which B. pertussis regulates virulence according to the stage

287 We encountered an adult patient in whom B. pertussis was isolated by culture who previously rece

288 cularly the infection of infant baboons with B. pertussis, are enabling longstanding questions about

289 eveloped severe disease when challenged with B. pertussis at 5 weeks of age.

290 pertussis (wP) vaccines and challenged with B. pertussis at 7 mo.

291 n to unvaccinated mothers were infected with B. pertussis at 5 weeks of age.

292 itical factor in establishing infection with B. pertussis and acts by specifically inhibiting the res

293 nteraction that is central to infection with B. pertussis and other Bordetella species.

294 expanded in the lungs during infection with B. pertussis and proliferated rapidly after rechallenge

295 d in the lungs of mice during infection with B. pertussis and significantly expanded through local pr

296 and memory induced by natural infection with B. pertussis.

297 Following inoculation with B. pertussis, but not B. parapertussis, IL-1R(-/-) mice

298 mit of detection was 3.0 x 10(5) CFU/mL with B. pertussis cells in buffer, 6.2 x 10(5) CFU/mL with na

299 ears, compared with 35% of 112 patients with B. pertussis infections (P = .001).

300 cells from the lungs of mice reinfected with B. pertussis produced significantly more IL-17 than gamm